Premium
Intrauterine Growth Restriction (IUGR) Induced by Reduced Uterine Perfusion in The Mouse Programs Impaired Glucose Homeostasis in Female Offspring
Author(s) -
Intapad Suttira
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.811.21
Subject(s) - medicine , endocrinology , offspring , intrauterine growth restriction , glucose homeostasis , impaired glucose tolerance , litter , birth weight , fetus , obesity , pregnancy , biology , insulin resistance , genetics , agronomy
Low birth weight is associated with increased risk of hypertension, obesity and metabolic diseases in later life but the mechanism is unclear. We previously showed IUGR in mouse programs hypertension. The aim of this study was to determine if IUGR in mice induced by placental insufficiency programs impaired metabolic health. Pregnant C57BL/6J mice were subjected to either a sham or a mechanical reduction of blood flow to the abdominal aorta, and both branches of ovarian arteries initiated at day13 of gestation to induce IUGR. Birth weight of the IUGR offspring was significantly lower than control (1.24±0.03 vs. 1.41±0.02 g, P<0.01; IUGR vs. control, respectively) but litter size was not different. Body weight, fat mass, lean mass, fasting blood glucose and intraperitonial glucose tolerance test (IPGTT) were not different upon comparison of IUGR to the same‐sex control at 6 or 14 weeks of age. At 34 weeks of age, body weight, body compositions, fasting blood glucose and IPGTT were similar between the male control and male IUGR. But female IUGR offspring showed a significant increase in fasting blood glucose as compared to female control (132.2±8.7 vs. 102.3±8.8 mg/dL, P<0.01; IUGR vs. control, respectively). IPGTT was significantly impaired in female IUGR (area under the curve: 1610±132 vs. 1229±46, P<0.01; IUGR vs. control, respectively), yet body weight and body composition were not different. This data suggests that IUGR in mouse programs metabolic disease in female offspring. The use of a mouse model of IUGR will allow for site and conditional genetic modifications to address novel hypotheses related to the developmental origins of chronic diseases. NIH: HL074927, HL51971, P20GM104357, AHA GRNT19900004